About: Renin-Angiotensin System and Coronavirus Disease 2019: A Narrative Review

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An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Renin-Angiotensin System and Coronavirus Disease 2019: A Narrative Review
Creator	Xia, Zhengyuan Rossi, Francesco Kassiri, Zamaneh Zhang, Shuyang Berrino, Liberato Capuano, Annalisa Paolisso, Giuseppe Racagni, Giorgio Scavone, Cristina Ferrajolo, Carmen Mascolo, Annamaria Rafaniello, Concetta
Source	Medline; PMC
abstract	Although clinical manifestations of the 2019 novel coronavirus disease pandemic (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-COV-2), are mainly respiratory symptoms, patients can also develop severe cardiovascular damage. Therefore, understanding the damage caused by SARS-COV-2 to the cardiovascular system and the underlying mechanisms is fundamental. The cardiovascular damage may be related to the imbalance of the renin-angiotensin-system (RAS) as this virus binds the Angiotensin-Converting-Enzyme 2 (ACE2), expressed on the lung alveolar epithelial cells, to enter into cells. Virus internalization may cause a downregulation of ACE2 on host cell surface that could lead to a local increased level of angiotensin II (AII) and a reduced level of angiotensin 1-7 (A1-7). An imbalance between these angiotensins may be responsible for the lung and heart damage. Pharmacological strategies that interfere with the viral attachment to ACE2 (umifenovir and hydroxychloroquine/chloroquine) or that modulate the RAS (analogous of A1-7 and ACE2, losartan) are in clinical development for COVID-19. The use of RAS inhibitors has also become a matter of public concern as these drugs may increase the mRNA expression and levels of ACE2 and impact the virulence and transmission of SARS-COV-2. Data on the effect of RAS inhibitors on ACE2 mRNA expression are scarce. Scientific societies expressed their opinion on continuing the therapy with RAS inhibitors in patients with COVID-19 and underlying cardiovascular diseases. In conclusion, RAS may play a role in SARS-COV-2-induced cardiac and pulmonary damage. Further studies are needed to better understand the role of RAS in COVID-19 and to guide decision on the use of RAS inhibitors.
has issue date	2020-08-11(xsd:dateTime)
bibo:doi	10.3389/fcvm.2020.00143
bibo:pmid	32850989
has license	cc-by
sha1sum (hex)	87916ef34222c62e61a15e27f81484f61ca831ec
schema:url	https://doi.org/10.3389/fcvm.2020.00143
resource representing a document's title	Renin-Angiotensin System and Coronavirus Disease 2019: A Narrative Review
has PubMed Central identifier	PMC7431661
has PubMed identifier	32850989
schema:publication	Front Cardiovasc Med
resource representing a document's body	covid:87916ef34222c62e61a15e27f81484f61ca831ec#body_text
is schema:about of	named entity 'adjusted odds ratio' named entity 'immune system disorders' named entity 'ACE2' named entity 'lung' named entity 'decompensation' named entity 'clinical trial' named entity 'nafamostat' named entity 'clinical trial' named entity 'ARBs' named entity 'inflammation' named entity 'endothelial cells' named entity 'AKI' named entity 'ARDS' named entity 'serine protease inhibitor' named entity 'umifenovir' named entity 'risk of death' named entity 'Narrative Review' named entity 'COVID-19' named entity 'disseminated intravascular coagulation' named entity 'antiviral' named entity 'MCP-1' named entity 'lopinavir/ritonavir' named entity 'reactive oxygen species' named entity 'COVID' named entity 'ACE2' named entity 'nausea' named entity 'fever' named entity 'COVID-19' named entity 'AII' named entity 'Enzyme' named entity 'ACE2' named entity 'COVID' named entity 'peptide' named entity 'SARS-COV-2' named entity 'COVID' named entity '84, 85' named entity 'diarrhea' named entity 'lung' named entity 'heart damage' named entity 'ACE2' named entity 'AT1' named entity 'risk factors' named entity 'viral infections' named entity 'infection' named entity 'RAS' named entity 'anti-hypertensive' named entity 'SARS-COV-2' named entity 'betacoronavirus' named entity 'respiratory symptoms' named entity 'COVID' named entity 'SARS' named entity '95% CI' named entity 'AII' named entity 'ACE2' named entity 'ACE inhibitor' named entity 'COVID' named entity 'SARS-COV-2' named entity 'ARDS' named entity 'lung tissue' named entity 'AII' named entity '95% CI' named entity 'infection' named entity 'chloroquine' named entity 'causal relationship' named entity 'cardiac diseases' named entity 'pro-inflammatory cytokines' named entity 'genome' named entity 'C-21' named entity 'DIC' named entity 'ACE2'

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